Date Thesis Awarded

5-2014

Document Type

Honors Thesis

Degree Name

Bachelors of Science (BS)

Department

Biology

Advisor

Eric L. Bradley

Committee Member

Margaret S. Saha

Committee Member

Daniel A. Cristol

Abstract

Mercury can disrupt the endocrine systems of mammals and fish, but little is known about its effects on the avian stress response. An experimental manipulation was used to show that methylmercury suppresses the stress-induced corticosterone response in birds, an effect previously unreported in the literature. Corticosterone regulates many normal metabolic processes, such as the maintenance of proper blood glucose levels during stressful daily fasting; an inability to increase corticosterone levels in response to stressors renders a bird less able to face a wide array of environmental challenges. Reproductively mature zebra finches that had been exposed to 0.0, 0.3, 0.6, 1.2, or 2.4 μg/g Hg (wet weight, ww) dietary methylmercury throughout their life (i.e. from the egg onwards) were the subjects of this study. In contrast to some field studies, no significant change in baseline plasma corticosterone concentrations was attributable to chronic methylmercury exposure. However, a comparison between the baseline corticosterone levels and levels after 30-minutes of handling stress revealed that the ability of birds to mount a stress response was reduced with increasing blood total mercury concentration. These results are consistent with adrenal corticoid disruption due to chronic mercury exposure, and mirror a similar study on free-living nestling songbirds exposed to environmental mercury. In addition, the glucocorticoid receptor in 50-day old juvenile zebra finches was studied to determine if this facet of the stress response pathway was also disrupted. No change was detected by quantitative PCR analysis in the expression of the glucocorticoid receptor in the brains of juvenile zebra finches. This result is consistent with the conclusion that mercury exposure does in fact have a significant effect on the stress response pathway, as the system is not compensating by altering receptor expression in response to abnormal hormone concentrations. More research will need to be done to determine whether the system is truly affected by mercury exposure, and whether or not it is compensating in some way for the disturbance of hormone concentrations. This project also studied the expression of the glucocorticoid receptor in zebra finch embryos of various stages, both through qPCR analysis and in situ hybridization. The purpose of studying embryos was not to compare expression among mercury treatment groups at this time, but rather to begin to characterize expression of the glucocorticoid receptor during the developmental stages of the Australian zebra finch, as there is currently no literature on this subject. The glucocorticoid receptor appears to be fairly ubiquitously expressed in zebra finch embryos from stage 17-30: more work will need to be done to continue the characterization of the expression of this receptor during the embryonic development of this species.

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